1Imaging Sciences Research Group,
University of Manchester, Manchester, United Kingdom; 2Faculty of
Life Sciences, University of Manchester, Manchester, United Kingdom; 3Institute
of Psychiatry, King's College London, London, United Kingdom; 4Neuroscience
& Psychiatry Unit, University of Manchester, Manchester, United Kingdom

Minocycline is
a safe, routinely prescribed broad-spectrum antibiotic effective against
neuro-inflammation and oxidative cell stress. These actions may mediate the
beneficial effects of minocycline on negative symptoms in schizophrenia.
Here, we show that pre-administration of minocycline induces widespread
attenuation of the ketamine-induced phMRI response. However, minocycline also
inhibited BOLD responses to electrical hindpaw stimulation, though cortical
local field potential changes were still present. These findings are
consistent with pharmacologically-induced disruption of neurovascular
coupling. These results are interpreted in the context of previous findings
linking minocycline to modulation of aberrant glutamate NMDA function.